Dioxins are a group of chemicals that share similar structures and ways of affecting the body. These compounds belong to three closely related families – the polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans (called furans), and certain polychlorinated biphenyls (PCBs). All dioxins are very stable and unlike most other chemicals do not quickly decompose or break down in the environment. Some of them have demonstrated adverse health effects in animals at very low levels. For this reason most countries are trying to reduce the amount of dioxins in the environment and people’s exposure to them.

Seventeen dioxins are thought to pose a health and environmental risk. The toxicity (or level of harmfulnes) of the 17 varies; 2,3,7,8-tetrachlorodibenzo-p-dioxin, abbreviated as 2,3,7,8-TCDD or TCDD and commonly referred to as dioxin, is the most toxic.

There are a few natural sources of dioxins, such as forest fires and volcanic activity, but most dioxins are from man made sources and are largely the result of formation as by-products of combustion (burning) and certain industrial processes. Advances in chemical and environmental management practices since the late 1980s have resulted in a reduction in dioxins emissions in New Zealand.

In 2004, New Zealand ratified the Stockholm Convention on Persistent Organic-Pollutants (POPs) the aim of which is to eliminate dioxins, where possible, from the environment.

Some exposure to dioxins is inevitable since they persist in the environment and are formed naturally as well as by certain industrial processes. Cigarette smoke also contains small amounts of dioxins. For most New Zealanders about 90 percent of dioxin exposure is through diet, mainly from foods that contain animal fats such as meat, dairy products, eggs and fish. Dioxins enter the food chain after being deposited onto soil and plant surfaces from the air and subsequently being eaten by grazing animals. Plants take up only very small amounts of dioxins via their roots. Small amounts of exposure occur from inhalation, skin absorption, and inadvertent ingestion of contaminated soil or dust.

Dioxins are broken down by exposure to sunlight, but if buried in the soil they are likely to remain there for a very long time. Once in the body dioxins accumulate in fat and persist for many years.

Typically lower levels of dioxins are found in people from less industrialised countries and in younger people. Levels for the New Zealand general population are at the low end of the range of levels reported internationally.

A study of the level of dioxin in the blood of 1834 New Zealanders conducted by the Ministry for the Environment in 1996-7 found the average amount of dioxin in blood was 2.7 pg/g (MfE, 2001) for people of the same age and sex as the Paritutu people tested. If projected to 2004 this represents a value of 1.7 pg/g. A picogram is a trillionth of a gram (0.000000000001g)

A study of the dioxins in the breast milk of a sample of New Zealand women, for the Ministry of Health, found the levels had decreased from an average of 16.4 pg/g of fat in breast milk in 1988 to 5.3 pg/g in 1998 – a fall of about 70 per cent over the decade. There was a further 40 percent decline from 1998 to 2008. The study of dioxins in breast milk was for all dioxins, not solely the TCDD dioxin found at elevated levels in the Paritutu blood serum study.

Despite many studies much is still not known about how dioxin affects humans and at what level exposed individuals might be likely to have health effects. How much dioxin the person is exposed to and for how long is important as well as individual susceptibility.

The most well studied dioxin is TCDD. At very high doses it may cause a severe acne-like skin condition known as chloracne and cancer in some people.

The adverse health effects associated with TCDD exposure are not yet fully known. Animal studies show immune, reproductive and developmental effects. Although the evidence of non-cancer effects in people is to date limited, these animal studies have been used internationally to establish health-based guidelines for exposure to dioxins in soil, air and food.

The first evidence that dioxin may cause cancer was an animal study published in 1978 but it was not till 1997 that dioxin was classified as a human carcinogen (cancer causing agent) by the International Agency for Research on Cancer (IARC).

In animal models TCDD appears to be a strong promoter (helps it along) and weak initiator (starter) of carcinogenesis (development of cancer). It is therefore possible that a carcinogenic (development of cancer) response to TCDD exposure in humans depends upon exposure to other initiators such as cigarette smoking.

The Institute of Medicine (IOM) of the National Academy of Sciences in the United States of America carries out regular reviews on all the evidence (animal and human) to create a list of conditions that are accepted as being associated with exposure to TCDD.

The conditions that have been accepted in the sufficient evidence of health effects category by the Institute of Medicine, are Hodgkin’s disease, non-Hodgkin’s lymphoma, soft tissue sarcoma, chronic lymphocytic leukaemia and chloracne.

There is no evidence to suggest that dioxin causes direct genetic damage. There is a small possibility that dioxin may cause indirect genetic damage.

Genetic testing of individuals will not provide any useful information in relation to their historic dioxin exposure. The difficulty in interpreting the results of genetic testing, and the inability to connect the results specifically to dioxin exposure need to be considered by people contemplating the test. There are no apparent clinical or prognostic benefits from genetic testing.

The former Ivon Watkins-Dow (IWD), now Dow AgroSciences (NZ) Ltd, chemical plant located in Paritutu, New Plymouth, manufactured the herbicide 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) from 1962 to 1987. Trichlorophenol (TCP), which is an intermediate in 2,4,5-T manufacture, was manufactured on site from 1969. During TCP manufacture, dioxin (TCDD) is formed and remains as a contaminant in 2,4,5-T. Production of 2,4,5-T ceased in 1987.

In October 2001 the Ministry of Health contracted the Institute of Environmental Science and Research Ltd (ESR) to investigate non-occupational exposure to dioxins among current and former Paritutu residents. Community consultation occurred between October 2001 and May 2002 resulting in agreement from the majority that blood serum testing was the appropriate mechanism for assessing this exposure. The report of this first phase was peer reviewed prior to its public release in March 2003.

A study protocol was then prepared for the next phase of the study and ethical approval obtained in May 2003 from the Taranaki Regional Ethics Committee. An interim report of the results from the first round of blood testing was released in September 2004. A final report which incorporated the second round of blood testing was released on 10 March 2005.

Advertisements were placed in the national and local media asking for people who had lived in Paritutu for more than one year in the 2,4,5-T production years to be a part of this study. To be included in the study, participants needed to have lived within a two kilometre radius east and one kilometre south of the former Ivon Watkins-Dow plant for at least one year between 1962 and 1987, and have no history of exposure in their working life to dioxins or significant period of residence outside New Zealand.

A potentially highly exposed group of current and former residents were then identified from this self-selected sample of the population based on spatial (where they lived in relation to the plant), toxicokinetic (the way dioxin behaves in the body of different age groups and both sexes) and multi-pathway exposure (different ways people may have been exposed) modelling.

The exposure model considered the place, and years of, residence in relation to various time periods.

Blood testing was undertaken in two rounds so that the results from the first round could assist in the selection of participants for the second round. This resulted in exclusion of people who lived in the area before 1974 from the second round in order to try to determine any variation in exposure from the IWD plant over time.

Blood was taken from 24 people in February 2004 and 28 people in October 2004 and the results were compared with those obtained in a national serum study carried out by the Ministry for the Environment (MfE) in 1996-7 which were projected to 2004 values. The people in the second group were younger on average than those in the first group and also their length of residence in Paritutu was shorter. Dioxin levels for the second group were higher on average than the NZ population but not as high as the first group.

Most of the exposure measured in 2004 happened through breathing the air between 18 and 43 years before, and significant exposure only happened to a small group of people living close to the plant for at least 15 years.

Results of the blood tests have been compared with data from a national study in 1997 which were projected to 2004 levels. This was done to ensure comparison of 2004 levels of TCDD with like levels from 1997. TCDD has an average half-life of 7 to 11 years which means the body excretes half of the amount of the dioxin in the body every 7 to 11 years. ESR took the 2004 levels and worked backwards to crudely estimate what the levels would have been when the residents were last exposed. In 1987 (or earlier if they left Paritutu) it is estimated the overall average increase in TCDD (above background) for the group of 52 participants was between at least 17 and 35 pg/g lipid. Among participants who lived in the area for at least 15 years, the peak increase above background was estimated to have been at least between 39 and 77 pg/g lipid. The individual with the highest measured exposure was estimated to be between 98 to 225 pg/g above background.

Currently, the average TCDD level for the 52 people who had blood samples taken is 6.5 picograms per gram of fat (pg/g lipid) and the expected national average for a group of similar age and sex is 1.7 pg/g lipid.

People who lived in the area for less than 15 years have an average level of 3.6 pg/g lipid, while people who lived in the area for at least 15 years have an average TCDD level of 14.7 pg/g.

The report from ESR states that the ‘elevations are in all probability due to breathing in emissions originating from the IWD plant.’ Eating ‘exposed’ fruit and vegetables (vegetables and fruit that is consumed without being peeled) was also a contributing factor. No relationship was found between TCDD levels and eating unexposed home grown vegetables and fruit, poultry/eggs or local seafood.

No specific time periods between 1962 and 1987 were identified as significant in relation to exposure. Subsequently, the study’s principal investigator has re-examined the data using information about dioxin half-lives that was not published when the ESR study was done. This suggests that exposure was most significant in the period 1965–1968.

Incinerator emissions do not explain the levels of exposure, which is unlikely to be from a single release of TCDD.

We now know with certainty that some people in the Paritutu community have in the past been exposed to TCDD at significantly higher levels than the typical New Zealand population. We anticipate there may be a small impact on cancer rates that we are unable to measure in a population this size. Our assumption is largely based on large population studies from overseas countries.

Responses to dioxin exposure differ among and within species, and among tissues in individual species. Because of the potential diversity of biological responses to dioxins in the body it is currently not possible to state how, or at what levels, exposed individuals will respond. How much dioxin the person is exposed to and for how long is important as well as individual susceptibility.

It is possible that the TCDD levels found may have adverse health consequences for individuals or may cause increased rates of disease, on a population basis. From studies that have been done to date on the Paritutu community, there is no clear indication of increased disease rates in the Paritutu population due to TCDD, although data limitations mean that a small increased risk cannot be excluded. Those data limitations include people who moved away from Paritutu not being able to be identified as former residents (and therefore included in the Ministry’s cancer study) from national health information databases such as the cancer registry. The extent of the cancer risk is highly uncertain but based on the evidence to date from the more highly exposed IARC occupational cohort and the Seveso general population cohort the Ministry of Health estimated in 2005 that for long term residents it may be up to 10% above the national all cancer mortality rate. This estimate was the maximum based on current scientific evidence that would occur under worst-case conditions.

One in three deaths among the New Zealand population every year are from cancer. The major risk factors for cancer in New Zealand are cigarette smoking and poor diet. Lung cancer and colorectal cancer each cause more than 1000 deaths per year.

If there were 100 people who lived in the highly exposed area of Paritutu for at least 15 years between 1962 to 1987, they might have up to a 10 % increase in their risk of dying from cancer, above their existing risk (which is 33 percent). Therefore if 100 people died in Paritutu every year about 33 deaths would be from cancer and up to an extra 3 cancer deaths may be attributable to dioxin. However these people would have had to have lived in the most exposed areas for at least 15 years from 1962 to 1987 or possibly in the period 1965 - 1968.

Since the ESR study was published further published studies from Seveso and on toxicokinetics support the conclusion that any increase in total cancer mortality is likely to be very small, most likely in the order of a few percent at most.

The blood TCDD levels estimated at the last time of exposure from three occupational cohorts are 2000 pg/g (mean) up to 32,000 pg/g, 1000 to 2400 pg/g, and 345-3890 pg/g. Each of these groups has shown an increased mortality (death rate) from all cancers combined.

A study of nine New Zealand 2,4,5-T applicators, with an average of 193 months spraying, found the average TCDD serum level (53.3 pg/g lipid) in 1988 was almost 10 times that for the matched control subjects (average 5.6 pg/g lipid). In general, the serum TCDD level increased with total duration of 2,4,5-T exposure. These applicators had sprayed 2,4,5-T for a range of 83 to 372 months and given the half-life of TCDD, the findings suggest that the increase in TCDD would be about 3 pg/g among workers who only sprayed for one year. The half-life is the time estimated for the body to excrete half of the dioxin it contains (estimated to be 7-11 years).

General population

These data may not be representative of the general population of these geographical areas.

Country

TCDD (pg/g lipid)

USA

5.2

Seveso, Italy (non-exposed)

4.9

Germany

3.6

South Vietnam

3.4 - 28

North Vietnam (Hanoi)

< 2.4

In some geographical areas other dioxins are a much greater contributor to total toxicity than TCDD. For example, toxic equivalents for all dioxins for Germany are similar to USA and two areas (Binh Hoa, Dong Nai) in South Vietnam despite lower TCDD levels.

Following the Seveso (Italy) industrial incident in 1976 three exposure zones were classified based on decreasing soil TCDD levels. Populations of the zones at the time of the incident were about 730 (highest exposure), about 5,900 (mid-range zone of exposure) and about 38,000 (low exposure). About 232,000 people from the surrounding non-exposed area have been followed up to serve as the reference population.

In 1996 (20 years later) the average TCDD results among randomly sampled exposed residents were 53.2 pg/g for those in the highest exposed zone and 11 pg/g in the mid-range exposed zone. This compares to 4.9 pg/g in the non-exposed zone. This study excluded people with severe medical illness and previous chloracne.

The mean Paritutu serum TCDD result of 14.7 pg/g for those who lived there at least 15 years from 1962 to 1987 is similar to some, but not as high as the highest, reported results found in areas of central and south Vietnam where aerial spraying of Agent Orange is known to have occurred about 20-28 years previously. It is slightly higher than the mid-range exposed zone of Seveso, 20 years after the incident.

The reports A Study of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Exposures in Paritutu, New Zealand August 2004 and February 2005 and accompanying appendices A-O were supplied to the Ministry of Health by the Institute of Environmental Science and Research Ltd (ESR).

The Ministry of Health cannot confirm the accuracy of the information and the analyses, and accepts no liability or responsibility for any acts or omissions, done or omitted in reliance, in whole or in part, on the data or the analyses.

As part of its contract with the Ministry of Health, ESR had the study independently peer reviewed. This helps to ensure that the study is of an appropriate high standard. Peer reviewers must be independent of a project and have appropriate subject matter and methodological knowledge.

In response to public concerns about the independence of ESR’s additional selected peer reviewers, the Ministry of Health sought recommendations from the World Health Organization and Dr Marie Haring Sweeney was selected as an independent peer reviewer.

A 2002 study of residential soil in the Paritutu area by the Ministry for the Environment found TCDD at all sites investigated, but all but one (from a grassed reserve on Mount Moturoa) result were below the most conservative international residential guidelines set to protect people’s health. The low levels measured mean that any risk to health of current and future residents from dioxin present in residential soil is negligible.

These soil findings are consistent with historical emissions from the plant as the source of TCDD in the area. The level of TCDD is normally low in relation to other dioxins when the primary source of dioxin is combustion. A previous MfE study, which was published in 1998, did not find TCDD in urban soils in any parts of the country other than New Plymouth.

The ESR report said concentrations tend to be highest close to the former IWD plant, and drop off rapidly within 800 to 1000 metres from the plant. Concentrations to the east of the plant, towards Mount Moturoa Domain, are higher than to the south of the plant. This is consistent with the prevailing winds in the area.

﻿Shouldn’t all people who have lived in Paritutu be tested now it is confirmed people were exposed?

Individual blood dioxins testing is not recommended.

Blood tests are usually used in order to accurately diagnose a disease so that the right kind of treatment can be started. In the case of testing for dioxins the results cannot be used to diagnose a disease. The results only tell us if the person has been exposed to dioxins. It cannot tell us if that person will get health effects or not because of the exposure.

Neither can blood tests for dioxins tell us what treatment to use as currently there is no generally accepted treatment available to eliminate dioxins from the body. Tests for measuring dioxins levels in people are not routinely available. These tests are costly, are carried out in only one New Zealand laboratory, and require a large amount of blood to be taken.

﻿What has been done to investigate the concerns of the Paritutu community?

Following community concern after a bursting disc failure at the plant in April 1986, the Minister of Health directed an Inquiry to be conducted. It found no substantiated evidence that 2,4,5-T manufacture had any adverse effect on residents’ health (Brinkman report 1986). It wasn’t till 1997 that TCDD was classified by the International Agency for Research on Cancer (IARC) as a human carcinogen.

In 2001, a group of government Ministers met and decided to implement an all-of-government approach to organochlorines (of which dioxin is one) issues in New Zealand because of the public concerns that had been raised.

The Ministry of Health was tasked with coordinating this group, which includes the Ministry for the Environment, ACC, the Department of Labour, Veterans Affairs, and the Ministry of Agriculture and Forestry and the New Zealand Food Safety Authority (these last two are now part of the Ministry for Primary Industries).

In September 2001, the Taranaki Regional Council released their report on alleged historical dumpsites used by the former IWD. No evidence of inappropriate disposal was found at any of the 36 separate sites investigated.

Also in September 2001, officials from the Ministry of Health and the Ministry for the Environment met with members of the Taranaki Regional Council, the New Plymouth District Council, the Taranaki District Health Board and its public health unit. It was agreed by all parties to take a coordinated approach to soil and blood testing.

In August 2001, Dr Patrick O’Connor, Medical Officer of Health for Taranaki, carried out a study in response to public concerns about health effects associated with living near the former IWD plant. No difference in cancer registrations (1990-97), and six percent (within the range of variation expected by chance) higher cancer mortality (1988-97) was found compared to the New Zealand population. The results do not exclude a small increased cancer risk.

In August 2002, Dr Patrick O’Connor released a report on birth defects data for 1965 – 1971 in response to concerns raised by data collected by a former nurse from Westown Maternity Hospital, New Plymouth. The rate of neural tube defects (spina bifida and anencephaly) was slightly higher than the estimated national rate but the difference is not statistically significant. Three cases were identified from an area near IWD – although this is two cases more than what was expected based on the New Plymouth rate the finding is of uncertain statistical significance because of problems with the data and definition of the study area.

In March 2005, the Ministry of Health released the serum dioxins report which found that people who had lived within 1km east and 400m south of the plant for at least 15 years during the years 2,4,5-T was manufactured which was from 1962 to 1987, were more likely to have higher levels of the dioxin TCDD than other New Zealanders.

In December 2005, the Ministry of Health released a study looking at cancer incidence and mortality in New Plymouth compared to the rest of New Zealand for the period 1970 to 2001 (see Does New Plymouth have higher rates of cancer?).

In 2002, the Medical Officer of Health for New Plymouth, Dr Patrick O’Connor conducted a study into the rate of birth defects notifications in New Plymouth. He found a lower rate of birth defects notifications (1988-99) compared to the New Zealand population.

The New Plymouth rate of neural tube defects (1965–72) was slightly higher than the estimated national rate but the difference was not statistically significant. Three cases were identified from an area near IWD, which is two cases more than what was expected based on the New Plymouth rate. Although not a statistically significant difference there are uncertainties with the data. Neural tube defects include spina bifida and anencephaly.

During 1965-1971, a midwife at Westown Maternity Hospital (WMH) in New Plymouth, collected data on the occurrence of birth defects in births in the hospital. These unpublished data have been used to compare the prevalences of birth defects in New Plymouth with those reported in other New Zealand hospital and population based national and local studies for the period prior to the establishment of the New Zealand Birth Defects Monitoring Programme (NZBDMP). During 1965-1971, the overall rate of birth defects, and specifically talipes and congenital dislocation of the hips (CHD), at the WMH was significantly higher that the rates reported from some other studies in New Zealand at that time. However, there was no difference between the rates of spina bifida, which has been associated with dioxin exposure.

From 1980 to 1989 NZBDMP data were used to compare the prevalences of birth defects in New Plymouth to those reported in other health districts. Data from the NZBDMP showed the rate of birth defects in New Plymouth was consistently higher than the national average and many other areas during 1980-1989. The difference was likely due to very high rates of CHD and talipes in New Plymouth. These defects are often caused by physical pressure in the womb from the way the baby lies or grows.

In late 2005 the Ministry of Health released a study looking at the number of people diagnosed with cancer and the number of people who have died from cancer in New Plymouth compared to the rest of New Zealand from 1970 to 2001.

The study was commissioned in response to community concerns about cancer because there is some evidence that exposure to dioxin can increase cancer risk. The evidence for an increased risk of all cancers combined is stronger than that for any specific cancer but there has been found to be an association between exposure to dioxin and four rare cancers, non-Hodgkin’s lymphoma, Hodgkin’s disease, soft tissue sarcoma and chronic lymphocytic leukaemia.

The study looked at the incidence (number of people diagnosed) and mortality from all cancers, as well as the incidence of and mortality from the four rare cancers in New Plymouth compared to the rest of New Zealand from 1970–2001, which includes the period that 2,4,5-T was manufactured in the region (1962–1987).

The study found that there was a slight downward trend for the number of people diagnosed with cancer and the number of people who had died as a result of cancer in New Plymouth compared to the rest of New Zealand for the period 1970 to 2001.

It found there was no evidence of an increased cancer risk related to the entire period of 2,4,5-T manufacture from 1962 to 1987, but the possibility of an undetected small elevation in cancer risk could not be excluded.

During one time period, 1970-1974 there was an elevated incidence for all cancers (total number of cases 876, expected number of cases 789; an 11% increase) non-Hodgkin’s lymphoma (total number of cases 33, expected number of cases 19; a 75% increase) and chronic lymphocytic leukaemia (total number of cases 16, expected number of cases 6; a 250% increase). This was followed in 1975-1979 by an increased death rate for non-Hodgkin’s lymphoma (24 deaths, expected number 15; a 58% increase).

However it is not possible to make any link between the higher rates during that limited period and dioxin exposure. Cancer usually takes more than 20 years to develop after an exposure, although there is some evidence that cancer may begin to develop as early as 10 years after dioxin exposure but even then it would put the critical period of exposure partially outside the manufacturing period for 2,4,5-T (1962-1987).

The authors of the study suggest that chance, unknown exposures or higher levels of fugitive emissions in the early manufacturing period are possible explanations.

While the study did not find evidence of an increased risk other than for 1970-1974 it does not rule out the existence of a small increase in risk. There were several limitations in this study. The population size is small, it is possible there was misclassification of some of the cancers, it was impossible to take into account people who have moved away and had cancer diagnosed in other parts of New Zealand and to analyse cancer data for the smallest statistical area including Paritutu due to boundary changes over time.

There is a special health service for people who were exposed to dioxins from the former Ivon Watkins- Dow factory in Paritutu, New Plymouth. You may be eligible for this service if you lived or worked at or near this factory between 1962 and 1987, and you are entitled to publicly funded services in New Zealand.

The Health Support Service for Dioxin Exposed People is for people who were exposed to dioxin from the former Ivon Watkins Dow factory in Paritutu, New Plymouth. This was established in 2008. It aims to help people stay healthy by promoting healthy lifestyles, reducing modifiable risk factors, and supporting the early detection of diseases.

Eligible people get a free annual health check from their doctor or practice nurse. Because every person’s health needs are different, your doctor or nurse will want to know what your needs are and make sure that you use services that help you stay healthy. Your health check depends on your medical history and current health needs.

The health check is free. All prescriptions, tests, or treatments will be funded as they normally are. Genetic counselling and serum dioxins testing will be free if you are referred. Other components of the Service are likely to be free or very low cost.

You will need to make an application to have your eligibility assessed. If you are eligible, you will be sent a letter (the confirmation of eligibility letter). When you get your confirmation of eligibility letter, you will need to make an appointment with your usual doctor. When you go for the appointment, you will need to give your confirmation of eligibility letter to the practice nurse or doctor. You will be sent a new confirmation of eligibility letter every year.

﻿Will I need to give any information to the Ministry of Health or my GP?

A database records information about people who apply for eligibility assessment. This database is used for communications and monitoring. It is managed by the Ministry of Health. Information will not be shared with other parties unless the explicit permision of individuals is granted.

No. You do not have to make an application. If you make an application and are assessed as being eligible but change your mind, you can decide at any time that you do not want to take part. If this happens, you will need to fill in a withdrawal form.

People can have their blood serum tested to see how much dioxin it contains today.

This test is not recommended. Serum dioxins tests cannot predict if a person will develop a disease, or the outcome of a disease that a person currently has. It cannot accurately tell what a person's past exposure was. A person who had a high level of exposure in the past may have a serum dioxins test which shows low or minimal levels of dioxin now. The amount of dioxin in a person’s body naturally decreases over time. How fast it decreases over time depends on many things including how old the person was when they were exposed, weight gain or loss, etc.

You have to have at least 90 millilitres of blood taken. The blood must be taken at a medical laboratory so that it can be quickly processed. The processed blood sample is then sent to a laboratory with the facilities to test for dioxins. The results of the test will be sent to your doctor. The doctor will discuss these results with you. Generally, the test can take some time to complete because it is complicated.

There is no generally accepted treatment to get rid of dioxins. Everyone has some dioxins in their body but levels in the general population are decreasing. Dioxin levels in the body reduce on average by half every 7 to 11 years as the dioxin is excreted.

Everyone has some dioxins in their body although levels in the general population are decreasing.

Reduction in the amount of animal fat in the diet reduces dioxins exposure although it is not recommended that all fat be eliminated from the diet, as a moderate amount is part of a healthy balanced diet. Not smoking and not burning rubbish, particularly plastics or driftwood, all help to reduce individual exposures.

What if I have some of the symptoms of these diseases or I am concerned about my health?

If my dioxin levels are elevated should I go to even greater lengths to limit my exposure in future?

What if I have some of the symptoms of these diseases or I am concerned about my health?

If you have concerns about your health you should consult your usual health practitioner. If you have concerns that you may have been exposed to dioxins you should advise your health practitioner so that can be taken into consideration in your health care.

All General Practitioners in New Plymouth and throughout New Zealand have been provided with information about the serum dioxins study and the known effects of dioxin.

If my dioxin levels are elevated should I go to even greater lengths to limit my exposure in future?

Yes. It is always wise to limit exposure to factors that present a risk to our health.

Previous studies of the New Zealand population show that dioxin levels have dropped since the late 1980s and this will continue to decline. It is estimated that 90 per cent of New Zealanders’ exposure comes through diet and as emissions to the environment decline New Zealanders’ exposure will continue to be reduced.

ACC: ACC will consider all claims for work-related dioxin exposure under Section 30 of the Injury Prevention, Rehabilitation and Compensation Act 2001. ACC will consider each situation carefully using all available relevant medical evidence to decide whether the person claiming has suffered a personal injury, and if so, whether there is a causal link between that personal injury and the exposure to dioxin in the work environment.